Classical hemifacial spasm (HFS) is in the majority of cases caused by cross-compression of the facial nerve near its entrance to the brainstem by a blood vessel, but its pathophysiology is largely unknown. Two hypotheses exist about the cause of HFS: 1) that it is ephaptic transmission between facial nerve fibers at the site of compression that causes spasm and synkinesis, and 2) that the facial motor nucleus is involved in producing the signs. We have earlier shown electrophysiological results from intraoperative recordings in patients undergoing microvascular decompression (MVD) operations for HFS. We found evidence that it is changes in structures that are central to the injury (probably the facial nucleus) rather than the injury to the nerve itself that give rise to the symptoms of HFS. We have also found evidence that ephaptic transmission between a small number of nerve fibers in the facial nerve at the site of lesion may occur under rare circumstances and for short periods of time when the facial nerve is being surgically manipulated, but it seems unlikely that such ephaptic transmission can generate the massive muscle contractions that are characteristic of HFS. In the proposed study we want to extend the intraoperative electrophysiological recordings in order to identify the location of the physiological abnormality that results in the spasm and abnormal muscle response. Animal experimentation will be done with the purpose of replicating HFS in an experimental animal. The rationale for the animal experimentation is that such a model will allow us to study directly the involvement of the facial motor nucleus. It may be assumed that the pathophysiology of other disorders caused by slightly injured nerves, such as various pain disorders, is similar to that of HFS, and we believe that patients with HFS provide a valuable model of other neurological disorders that are caused by slightly injured nerves.